Type 1 diabetes (T1D) is an autoimmune disease in which reaction to specific self-antigens results in the destruction of pancreatic insulin-producing β cells by antigen-specific antibodies and cytotoxic T lymphocytes (CTLs). There is no cure for T1D, and the only treatment options currently available are insulin and/or cell therapy. A variety of methods are currently under development for treating T1D by inhibiting autoimmunity. These include systemic immunosuppression, activation or inhibition of specific immune signaling pathways, and infusion of specific regulatory cell populations (Herold 2013; Coombes 2007).
One of the most promising approaches for preventing β cell autoimmune destruction is vaccination with diabetic autoantigens, which can result in inhibition of destructive islet-specific responses and induction of regulatory responses (Holmgren 2005; Peakman 2010; Nicholas 2011). In certain cases, autoantigen vaccination has been combined with administration of cytokines, which may synergize with the antigen-specific effect (Denes 2006; Denes 2010). The autoantigens proinsulin and GAD65 have both proven to be effective in reversing and preventing diabetes in non-obese diabetic (NOD) mouse models of T1D. However, human clinical trials using these autoantigens have been disappointing.